Airway Management Flashcards

1
Q

What is the acceptable extubation failure rate?

A

10-20%
An re-intubation rate < 10 may indicate too conservative as approach
A re-intubation rate > 20 may indicate premature extubations

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2
Q

What are the criteria for weaning and extubating a patient?

A

A - patent. If in doubt check for cuff leak or look down.
B - minimal oxygenation supporr FiO2 < 0.4, PEEP < 8, adequate ventilatory drive, ability to clear secretions
C - haemodynamic stability
D - sufficient consciousness to protect airway
E - original pathology resolved, no impending procedures under GA/sedation

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3
Q

What factors suggest failure of a spontaneous breathing trial?

A
Physiological
Hr > 20% increase or > 140
SBP > 20% baseline or >180/<90
Cardiac arrhythmias
Resp rate > 50% BASELINE OR > 35
pAo2 < 8 ON fIo2 >0.5
pAco2 >6.5
pH < 7.32
Clinical
Agitation or anxiety
Depressed mental state
Sweating/cyanosis
Increased resp effort
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4
Q

What are the risk factors for failing extubation?

A
Age > 65
Underlying chronic cardiorespiratory disease
Heart failure / LV dysfunction
COPD
OSA/obesity
PaCO2 > 6.5
Neuromuscular disorders
Positive fluid balance
Ventilation > 6 days
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5
Q

How many ICU patients experience post extubation stridor? What are the risk factors?

A
16%
Female
Muscle weakness
Tracheal infection
TRacheal stenosis
Recent airway surgery
Intubation > 36 hours
Excessive cuff pressures
Large ETT
Aggressive suctioning
NGT insertion
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6
Q

What are the indications for tracheostomy in ICU patients?

A

Inability to maintain upper airway - primary pathology or neurological impairment
Prolonged ventolator wean
Inability to adequately clear secretions

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7
Q

What are the potential advantages of trache over ETT?

A

Shorter tube - reduced dead space, reduced resistance to gas flow, reduced work of breathing, easier access for suctioning
Reduced need for sedation - improved cough and secretion clearance, improved communication, better compliance with physio
Avoidance of ETT - better mouth care, potential for speech, potential to eat

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8
Q

What are the contra-indications for tracheostomy?

A

Local - anatomical abnormalities, infection over insertion site, known or suspected difficult ETT, short neck, obesity, unstable spinal injury
Systemic - coagulopathy, significant haemodynamic instbaility, significant resp support (FiO2 >0.6, PEEP >10), inability to tolerate changes in PaCO2 (e.g. raised ICP)

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9
Q

What are the complications of a tracheostomy?

A

Immediate - hypoxia, hypercarbia, loss of airway, aspiration, haemorrhage, damage to local structures, anaesthesia related e.g. anaphylaxis, hypotension
Early - infection, displacement with loss of airway, occlusion, tracheal injury, haemorrhage (mucosal injury or erosion into right brachiocephalic artery)
Late - tracheal dilatation, tracheomalacia, tracheal stenosis

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10
Q

What are the indications for bronchoscopy?

A

Diagnostic - broncho-alveolar lavage, biopsy, assessment of inhalational injury, confirm ETT position
Therapeutic- removal of bronchial obstruction, placement of bronchial stent
Assist invervention - FOI, perc trache, DLT insertion, positioning of endobronchial blocker

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11
Q

What is ARDS?

A

An inflammatory process affecting the lungs
Initial injury precipitates a sequence of events manifesting as impaired oxygenation, impaired compliance and increased dead space
It has 3 phases - exudative, proliferative, and fibrosing

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12
Q

What is the definition of ARDS?

A

Defined by the Berlin criteria
Timing - Occurs within 1 week of a known clinical insult
Chest imaging - bilateral opacities on CXR
Origin of oedema - resp failure not fully explained by cardiac failure or fluid overload
Moderate-to-severe hypoxia - defined by the PaO2/FiO2 ratio on a ventilator with >5cmh2o PEEP.
p:f < 39.9 > 26.6 = mild
p:f < 26.6 > 13.3 = moderate
p:f < 13.3 = severe

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13
Q

What is the differential diagnosis of ARDS?

A

Cardiogenic pulmonary oedema
Acute eosinophilic pneuimonia
Cryptogenic organizing pneumonia
Diffuse alveolar haemorrhage

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14
Q

What is the aetiology of ARDS?

A

Direct - pnuemonia, viral pnuemonitis, chemical pnuemonitis, smoke inhalation, near drowning, pulmonary contusions, reperfusion injury, thoracic radiation
Indirect - systemic sepsis, major trauma, pancreatitis, pregnancy-related, TRALI, tumour lysis syndrome

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15
Q

What are the general management strategies for ARDS?

A

Sedation - improves mechanical ventilation compliance and decreases O2 consumption
Neuromuscular blockade -improves compliance and decreases O2 consumption - not without complication - but there is evidence that they may decrease mortality if used early on in severe ARDS
Fluid balance - conservative strategy leads to improved lung function and reduced number of days on the ventilator but no decrease in mortality
House-keeping - infection control, DVT prophylaxis, Ulcer prophylaxis and nutrition

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16
Q

What ventilator strategies should be employed in ARDS?

A

Low tidal volume 6ml/kg, significantly decreases mortality vs 12ml/kg
Maintain plateau pressure < 30cnH2O
High PEEP - decreasing atelectotrauma - may improve mortality in those with severe ARDS
Recruitment maneauvres - no evidence to show improved outcomes
Permissive hypercapnia - acceptance of increased co2 and acidosis

17
Q

Discuss the role of steroids in ARDS

A

Theoretically beneficial given inflammatory nature
Appear to increase oxygenation and number of ventilator free days
Given between days 7-13 may be associate with improved mortality, however late may increase mortality

18
Q

Discuss the role of beta agonists in ARDS

A

Reduce extravascular lung water

No evidence on improved outcomes

19
Q

What is the role of statins in ARDS?

A

Small study showed improvement in non-pulmonary organ dysfunction, larger study showed no benefit

20
Q

What is the role of nitric oxide in ARDS?

A

Inhaled NO selectively vasoldilates those pulmonary vessels serving ventilated lung. Improves oxygenation but no evidence for improved outcomes

21
Q

What are the mechanisms of inhalational injury?

A

Heat - causes oedema, eryhtema, and mucosal ulceration
Toxins- sulphur dioxide, chlorine, ammonia
Environmental hypoxia due to oxygen consumption

22
Q

What is the pahophysiology pf inhalational injury?

A

Exudative phase - characterised by neutrophil influx, macrophage activation, increased permeability, type 2 pneumocyte dysfucntion and decreased surfactant production
Fibrotic phase - fibrosing alveolitis, neoangiogenesis collagen deposition

23
Q

What signs are associated with airway burns?

A

Facial or muscoal burns, singeing of nasal hair, hoarse voice, carbonaceous sputum

24
Q

What effect does carbon monoxide have?

A

Binds to Hb with 250 times the affinity of oxygen
Causes left shift of OHDC
Cellular cytochrome oxidase system is inhibited
Results in tissue hypoxia

25
Q

How do you diagnose carbon monoxide poisoning?

A

Pulse oximeters cannot distinguish between oxyhaemoglobin and carboxyhaemoglobin and therefore and ABG is required
A level > 10% in problematic
>25% will require ventilation
>40% - consider hyperbaric oxygen

26
Q

What are the effects of cyanide?

A

Binds to the ferric ion on cytochrome oxidase, blocking aerobic cellular metabolism

27
Q

What are the clinical features of cyanide toxicity?

A

Hypoxia

Lactic acidosis

28
Q

How is cyanide toxicity treated?

A

Binding of cynaide with hydroxycobalamin or dicobalt edatate
Or induction of methaemoglobinaemia with amyl nitrate or sodium nitrate. The resultant ferric ion provides an alternative binding site for cyanide
Or sulphur donor sodium thiosulphate with converts cyanide to the inert and renally excreted thiocyanate